TY - JOUR
T1 - Thyrotropin decreases leptin production in rat adipocytes
AU - Shintani, Mitsuyo
AU - Nishimura, Haruo
AU - Akamizu, Takashi
AU - Yonemitsu, Shin
AU - Masuzaki, Hiroaki
AU - Ogawa, Yoshihiro
AU - Hosoda, Kiminori
AU - Inoue, Gen
AU - Yoshimasa, Yasunao
AU - Nakao, Kazuwa
N1 - Funding Information:
From the Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, Japan. Submitted February 19, 1999; accepted June 28, 1999. Supported in part by grants from the Japanese Ministry of Education, Science, and Culture, the Japanese Ministry of Health and Welfare, and the Insulin Research Foundation. Address reprint requests to Haruo Nishimura, MD, PhD, Laboratory of Diabetes and Obesity, Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sal~o-ku, Kyoto 606-8507, Japan. Copyright © 1999 by W.B. Saunders Company 0026-0495/99/4812-0020510.00/0
PY - 1999
Y1 - 1999
N2 - Leptin, which is secreted from adipocytes, has a role in the regulation of appetite and energy expenditure. The thyrotropin receptor (TSH-R) was recently found in adipocytes. We examined the effects of TSH on leptin production and lipolysis in rat epididymal adipocytes. TSH decreased the concentration of leptin in the medium time (~24 hours), and dose (~10-7 mol/L)-dependently (half-maximal inhibition [IC50] ≃ 10-9 mol/L). TSH also decreased the ob mRNA level approximately 55% in adipocytes. We confirmed the presence of TSH-R mRNA in the adipocytes by reverse transcription-polymerase chain reaction (RT-PCR). TSH stimulated glycerol release dose-dependently (IC50 ≃ 10-8 mol/L) in adipocytes. This TSH- induced glycerol release was further enhanced by adenosine deaminase (ADA). In summary, TSH reduced leptin production and stimulated lipolysis in rat epididymal adipocytes. Although the pathophysiological relevance of the regulation of leptin production and lipolysis by TSH is unknown, we speculate that TSH may affect the regulation of appetite and energy expenditure in pathophysiological states.
AB - Leptin, which is secreted from adipocytes, has a role in the regulation of appetite and energy expenditure. The thyrotropin receptor (TSH-R) was recently found in adipocytes. We examined the effects of TSH on leptin production and lipolysis in rat epididymal adipocytes. TSH decreased the concentration of leptin in the medium time (~24 hours), and dose (~10-7 mol/L)-dependently (half-maximal inhibition [IC50] ≃ 10-9 mol/L). TSH also decreased the ob mRNA level approximately 55% in adipocytes. We confirmed the presence of TSH-R mRNA in the adipocytes by reverse transcription-polymerase chain reaction (RT-PCR). TSH stimulated glycerol release dose-dependently (IC50 ≃ 10-8 mol/L) in adipocytes. This TSH- induced glycerol release was further enhanced by adenosine deaminase (ADA). In summary, TSH reduced leptin production and stimulated lipolysis in rat epididymal adipocytes. Although the pathophysiological relevance of the regulation of leptin production and lipolysis by TSH is unknown, we speculate that TSH may affect the regulation of appetite and energy expenditure in pathophysiological states.
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U2 - 10.1016/S0026-0495(99)90247-0
DO - 10.1016/S0026-0495(99)90247-0
M3 - Article
C2 - 10599990
AN - SCOPUS:13044300890
SN - 0026-0495
VL - 48
SP - 1570
EP - 1574
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 12
ER -
